[The stereology of the myocardium in rats hypertensive due to the use of an inhibitor of nitric oxide synthesis].
OBJECTIVE
To study, with stereology, the myocardial changes in experimental arterial hypertension induced by chronic inhibition of nitric oxide synthesis.


METHODS
Two groups of 10 young normotensive adult rats (Wistar Strain) were studied, control and L-Name groups. In the L-Name group, the animals received 60 mg/100 ml (equivalent to 12 mg/animal) of L-Name daily in their drinking water. After 40 days, the animals were sacrificed and their hearts excised and weighed. Several myocardial fragments were taken from the free wall of the left ventricle, fixed in buffered 10% formalin and prepared for light microscopic study. Sections were stained by H-E, Gieson's Trichrome, Weigert's resorcin-fucsin and picro Sirius. Sixteen microscopic random fields were studied in each heart. The myocardium was considered to be composed of myocytes and cardiac interstitium (with blood vessels and connective tissue). Stereological parameters were volume, length and surface densities as well as the absolute values of these parameters. The differences between the animals in the control group and the L-Name group were tested with the non-parametric Mann-Whitney test.


RESULTS
The main changes in the myocardium of the L-Name group were interstitial and perivascular fibrosis and myocyte hypertrophy. In the L-Name group, blood pressure was 94.5% greater and cardiac weight 35.8% greater than in the control group (p < 0.05). The following differences were significant between the control group and the L-Name group: length, density of the blood vessels, surface densities of myocytes and blood vessels (16%, 21.2% and 40.7% smaller in the L-Name group than in the control group, respectively). The mean cross sectional area of the myocytes, the absolute volumes of the blood vessels and connective tissue were greater in the L-Name group than in the control group (41.1%, 44.6% and 38.6%, respectively). In this study, the stereological determinations for the blood vessels were smaller in the myocardium of the L-Name group than in the control group. This suggests that in L-Name myocardium hypertrophy the proliferation of blood vessels is not marked.


CONCLUSIONS
Chronic inhibition of nitric oxide synthesis significantly changes the myocardium with hypertrophy of the myocytes and fibrosis. The change in the myocardial microvasculature of the L-Name group is demonstrated by the decrease in both length and surface densities of the blood vessels.
Pereira
L M
LM
Universidade do Estado do Rio de Janeiro, Laboratório de Morfometria e Morfologia Cardiovascular.
Mandarim-de-Lacerda
C A
CA
D000818:Animals; D004791:Enzyme Inhibitors; D006321:Heart / Q000187:drug effects*; D006973:Hypertension / Q000139:chemically induced / Q000473:pathology*; D008297:Male; D009206:Myocardium / Q000473:pathology*; D019331:NG-Nitroarginine Methyl Ester; D009569:Nitric Oxide / Q000037:antagonists & inhibitors*; D051381:Rats; D017208:Rats, Wistar; D018709:Statistics, Nonparametric
D004791:Enzyme Inhibitors; D009569:Nitric Oxide; D019331:NG-Nitroarginine Methyl Ester
Estereologia do miocárdio em ratos hipertensos pelo uso de inibidor da síntese do óxido nítrico.